Evidence map›Paper›PMID 31242179›Full record

ArticlePLoS biology2019

Inferring the distribution of fitness effects of spontaneous mutations in Chlamydomonas reinhardtii.

Katharina B Böndel, Susanne A Kraemer, Toby Samuels, Deirdre McClean, Josianne Lachapelle, Rob W Ness, Nick Colegrave, Peter D Keightley

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 64 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Katharina B BöndelInstitute of Evolutionary Biology, Ashworth Laboratories, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0001-8919-729X
Susanne A KraemerInstitute of Evolutionary Biology, Ashworth Laboratories, University of Edinburgh, Edinburgh, United Kingdom.
Toby SamuelsInstitute of Evolutionary Biology, Ashworth Laboratories, University of Edinburgh, Edinburgh, United Kingdom.
Deirdre McCleanInstitute of Immunology and Infection Research, Ashworth Laboratories, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0002-5857-9081
Josianne LachapelleDepartment of Biology, William G. Davis Building, University of Toronto, Mississauga, Canada.ORCID 0000-0001-8164-6361
Rob W NessDepartment of Biology, William G. Davis Building, University of Toronto, Mississauga, Canada.ORCID 0000-0001-7313-8236
Nick ColegraveInstitute of Evolutionary Biology, Ashworth Laboratories, University of Edinburgh, Edinburgh, United Kingdom.
Peter D KeightleyInstitute of Evolutionary Biology, Ashworth Laboratories, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0001-8129-2794
University of Edinburgh · GBUniversity of Toronto · CACentre for Immunity, Infection and Evolution · GBConcordia University · CA

Funding

Biotechnology and Biological Sciences Research Council RA2644
6 · The paper itself

Abstract

Spontaneous mutations are the source of new genetic variation and are thus central to the evolutionary process. In molecular evolution and quantitative genetics, the nature of genetic variation depends critically on the distribution of effects of mutations on fitness and other quantitative traits. Spontaneous mutation accumulation (MA) experiments have been the principal approach for investigating the overall rate of occurrence and cumulative effect of mutations but have not allowed the phenotypic effects of individual mutations to be studied directly. Here, we crossed MA lines of the green alga Chlamydomonas reinhardtii with its unmutated ancestral strain to create haploid recombinant lines, each carrying an average of 50% of the accumulated mutations in a large number of combinations. With the aid of the genome sequences of the MA lines, we inferred the genotypes of the mutations, assayed their growth rate as a measure of fitness, and inferred the distribution of fitness effects (DFE) using a Bayesian mixture model. We infer that the DFE is highly leptokurtic (L-shaped). Of mutations with absolute fitness effects exceeding 1%, about one-sixth increase fitness in the laboratory environment. The inferred distribution of effects for deleterious mutations is consistent with a strong role for nearly neutral evolution. Specifically, such a distribution predicts that nucleotide variation and genetic variation for quantitative traits will be insensitive to change in the effective population size.

Indexed as

Mutation AccumulationBayes TheoremBiological EvolutionChlamydomonas reinhardtiiDNA Mutational AnalysisEvolution, MolecularGenetic FitnessGenetic VariationGenotypeModels, GeneticMutagenesisMutationMutation RateSelection, Genetic

Identifiers

PMID31242179
PMCPMC6615632
OpenAlexW2955519173

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.